Silica coatings on young Hawaiian basalts: Constraints on formation mechanism from silicon isotopes

Young basalts from Kilauea, on the big island of Hawai’i, frequently feature visually striking, white, orange and blue coatings, consisting of a 10-50 μm layer of amorphous silica, capped, in some cases, by a ~1 μm layer of Fe-Ti oxide [1]. The coatings provide an opportunity to study the early onset of acid-sulfate weathering, a process common to many volcanic environments. Silicon isotopes fractionate with the precipitation of clays and opaline silica, and have been demonstrated to be an indicator of weathering intensity [2,3]. Here we report in situ measurements of δ^(30)_Si of the silica coatings and their implications for coating formation

Independent Validation of the SWMM Green Roof Module

Green roofs are a popular Sustainable Drainage Systems (SuDS) technology. They provide multiple benefits, amongst which the retention of rainfall and detention of runoff are of particular interest to stormwater engineers. The hydrological performance of green roofs has been represented in various models, including the Storm Water Management Model (SWMM). The latest version of SWMM includes a new LID green roof module, which makes it possible to model the hydrological performance of a green roof by directly defining the physical parameters of a green roof’s three layers. However, to date, no study has validated the capability of this module for representing the hydrological performance of an extensive green roof in response to actual rainfall events. In this study, data from a previously-monitored extensive green roof test bed has been utilised to validate the SWMM green roof module for both long-term (173 events over a year) and short-term (per-event) simulations. With only 0.357% difference between measured and modelled annual retention, the uncalibrated model provided good estimates of total annual retention, but the modelled runoff depths deviated significantly from the measured data at certain times (particularly during summer) in the year. Retention results improved (with the difference between modelled and measured annual retention decreasing to 0.169% and the Nash-Sutcliffe Model Efficiency (NSME) coefficient for per-event rainfall depth reaching 0.948) when reductions in actual evapotranspiration due to reduced substrate moisture availability during prolonged dry conditions were used to provide revised estimates of monthly ET. However, this aspect of the model’s performance is ultimately limited by the failure to account for the influence of substrate moisture on actual ET rates. With significant differences existing between measured and simulated runoff and NSME coefficients of below 0.5, the uncalibrated model failed to provide reasonable predictions of the green roof’s detention performance, although this was significantly improved through calibration. To precisely model the hydrological behaviour of an extensive green roof with a plastic board drainage layer, some of the modelling structures in SWMM green roof module require further refinement

The dumortierite supergroup. I. A new nomenclature for the dumortierite and holtite groups

Although the distinction between magnesiodumortieite and dumortierite, i.e. Mg vs. Al dominance at the partially vacant octahedral Al1 site, had met current criteria of the IMA Commission on New Minerals, Nomenclature and Classification (CNMNC) for distinguishing mineral species, the distinction between holtite and dumortierite had not, since Al and Si are dominant over Ta and (Sb, As) at the Al1 and two Si sites, respectively, in both minerals. Recent studies have revealed extensive solid solution between Al, Ti, Ta and Nb at Al1 and between Si, As and Sb at the two Si sites or nearly coincident (As, Sb) sites in dumortierite and holtite, further blurring the distinction between the two minerals. This situation necessitated revision in the nomenclature of the dumortierite group. The newly constituted dumortierite supergroup, space group Pnma (no. 62), comprises two groups and six minerals, one of which is the first member of a potential third group, all isostructural with dumortierite. The supergroup, which has been approved by the CNMNC, is based on more specific end-member compositions for dumortierite and holtite, in which occupancy of the Al1 site is critical. (1) Dumortierite group, with Al1 = Al^(3+), Mg^(2+) and 〈, where 〈 denotes cation vacancy. Charge balance is provided by OH substitution for O at the O2, O7 and O10 sites. In addition to dumortierite, endmember composition AlAl_6Bsi_3O_(18), and magnesiodumortierite, endmember composition MgAl_6Bsi_3O_(17)(OH), plus three endmembers, “hydroxydumortierite”, 〈Al_6Bsi_3O_(15)(OH)_3 and two Mg-Ti analogues of dumortierite, (Mg_(0.5)Ti_(0.5))Al_6Bsi_3O_(18) and (Mg_(0.5)Ti_(0.5))Mg_2Al_4Bsi_3O_(16)(OH)_2, none of which correspond to mineral species. Three more hypothetical endmembers are derived by homovalent substitutions of Fe^(3+) for Al and Fe^(2+) for Mg. (2) Holtite group, with Al1 = Ta^(5+), Nb^(5+), Ti^(4+) and 〈. In contrast to the dumortierite group, vacancies serve not only to balance the extra charge introduced by the incorporation of pentavalent and quadrivalent cations for trivalent cations at Al1, but also to reduce repulsion between the highly charged cations. This group includes holtite, endmember composition (Ta_(0.6)〈_(0.4))Al_6Bsi_3O_(18), nioboholite (2012-68), endmember composition (Nb_(0.6)〈_(0.4_)Al_6Bsi_3O_(18), and titanoholtite (2012-69), endmember composition (Ti_(0.75)〈_(0.25))Al_6Bsi_3O_(18). (3) Szklaryite (2012-70) with Al1 = 〈 and an endmember formula 〈Al_6Bas^(3+)_ 3O_(15). Vacancies at Al1 are caused by loss of O at O2 and O7, which coordinate the Al1 with the Si sites, due to replacement of Si^(4+) by As^(3+) and Sb^(3+), and thus this mineral does not belong in either the dumortierite or the holtite group. Although szklaryite is distinguished by the mechanism introducing vacancies at the Al1 site, the primary criterion for identifying it is based on occupancy of the Si/As, Sb sites: (As^(3+) + Sb^(3+)) > Si^(4+) consistent with the dominant-valency rule. A Sb^(3+) analogue to szklaryite is possible

The dumortierite supergroup. II. Three new minerals from the Szklary pegmatite, SW Poland: Nioboholtite, (Nb_(0.6)〈_(0.4))Al_6Bsi_3O_(18), titanoholtite, (Ti_(0.75)〈_(0.25))Al_6Bsi_3O_(18), and szklaryite 〈Al_6Bas^(3+)_ 3O_(15)

Three new minerals in the dumortierite supergroup were discovered in the Szklary pegmatite, Lower Silesia, Poland. Nioboholtite, endmember (Nb_(0.6)〈_(0.4))Al_6B_3Si_3O_(18), and titanoholtite, endmember (Ti_(0.75)〈_(0.25))Al_6B_3Si_3O_(18), are new members of the holtite group, whereas szklaryite, endmember 〈Al_6Bas^(3+)_ 3O_(15), is the first representative of a potential new group. Nioboholtite occurs mostly as overgrowths not exceeding 10 μm in thickness on cores of holtite. Titanoholtite forms patches up to 10 μm across in the holtite cores and streaks up to 5 μm wide along boundaries between holtite cores and the nioboholtite rims. Szklaryite is found as a patch ∼2 μm in size in As- and Sb- bearing dumortierite enclosed in quartz. Titanoholtite crystallized almost simultaneously with holtite and other Ta-dominant minerals such as tantalite-(Mn) and stibiotantalite and before nioboholtite, which crystallized simultaneously with stibiocolumbite during decreasing Ta activity in the pegmatite melt. Szklaryite crystallized after nioboholtite during the final stage of the Szklary pegmatite formation. Optical properties could be obtained only from nioboholtite, which is creamy-white to brownish yellow or grey-yellow in hand specimen, translucent, with a white streak, biaxial (–), n_α = 1.740 – 1.747, n_β ∼ 1.76, n_γ ∼ 1.76, and Δ < 0.020. Electron microprobe analyses of nioboholtite, titanoholtite and szklaryite give, respectively, in wt.%: P_2O_5 0.26, 0.01, 0.68; Nb_2O_55.21, 0.67, 0.17; Ta_2O_5 0.66, 1.18, 0.00; SiO_2 18.68, 21.92, 12.78; TiO_2 0.11, 4.00, 0.30; B_2O_3 4.91, 4.64, 5.44; Al_2O_3 49.74, 50.02, 50.74; As_2O_3 5.92, 2.26, 16.02; Sb_2O_3 10.81, 11.48, 10.31; FeO 0.51, 0.13, 0.19; H_2O (calc.) 0.05, –, –, Sum 96.86, 96.34, 97.07, corresponding on the basis of O = 18–As–Sb to {(Nb_(0.26)Ta_(0.02)〈_(0.18)) (Al_(0.27)Fe_(0.05)Ti_(0.01))〈_(0.21)}_(Σ1.00)Al_6B_(0.92){Si_(2.03)P_(0.02)(Sb_(0.48)As_(0.39)Al_(0.07)}_(Σ3.00)(O_(17.09)OH_(0.04)〈_(0.87))_(Σ18.00), {(Ti_(0.32) Nb_(0.03)Ta_(0.03)〈_(0.10) )(Al_(0.3 5) Ti_(0.01) Fe_(0.01))〈_(0.15)}_(Σ1.00) Al_6 B_(0.86) {Si_(2.36) (Sb_(0.51) As_(0.14) )}_(Σ3.01)(O_(17.35)〈_(0.65))_(Σ18.00) and {〈_(0.53) (Al_(0.41) Ti_(0.02) Fe_(0.02))(Nb_(0.01)〈_(0.01) )}_(Σ1.00)Al_6 B_(1.01) {(As_(1.07) Sb_(0.47) Al_(0.03)) Si_(1.37) P_(0.06)}_(Σ3.00)(O_(16.46)〈_(1.54))_(Σ18.00). Electron backscattered diffraction indicates that the three minerals are presumably isostructural with dumortierite, that is, orthorhombic symmetry, space group Pnma (no. 62), and unit-cell parameters close to a = 4.7001, b = 11.828, c = 20.243 Å, with V = 1125.36 Å^3 and Z = 4; micro-Raman spectroscopy provided further confirmation of the structural relationship for nioboholtite and titanoholtite. The calculated density is 3.72 g/cm^3 for nioboholtite, 3.66 g/cm^3 for titanoholtite and 3.71 g/cm^3 for szklaryite. The strongest lines in X-ray powder diffraction patterns calculated from the cell parameters of dumortierite of Moore and Araki (1978) and the empirical formulae of nioboholtite, titanoholtite and szklaryite are [d, Å, I (hkl)]: 10.2125, 67, 46, 19 (011); 5.9140, 40, 47, 57 (020); 5.8610, 66, 78, 100 (013); 3.4582, 63, 63, 60 (122); 3.4439, 36, 36, 34 (104); 3.2305, 100, 100, 95 (123); 3.0675, 53, 53, 50 (105); 2.9305, 65, 59, 51 (026); 2.8945, 64, 65, 59 (132), respectively. The three minerals have been approved by the IMA CNMNC (IMA 2012-068, 069, 070) and were named for their relationship to holtite and occurrence in the Szklary pegmatite, respectively

Lead-tellurium oxysalts from Otto Mountain near Baker, California, USA: XII. Andychristyite, PbCu^(2+)Te^(6+)O_5(H_2O), a new mineral with hcp stair-step layers

Andychristyite, PbCu^(2+)Te^(6+)O_5(H_2O), is a new tellurate mineral from Otto Mountain near Baker, California, USA. It occurs in vugs in quartz in association with timroseite. It is interpreted as having formed from the partial oxidation of primary sulfides and tellurides during or following brecciation of quartz veins. Andychristyite is triclinic, space group P1, with unit-cell dimensions a = 5.322(3), b = 7.098(4), c = 7.511(4) Å, α = 83.486(7), β = 76.279(5), γ = 70.742(5)°, V = 260.0(2) Å^3 and Z = 2. It forms as small tabular crystals up to ∼50 µm across, in sub-parallel aggregates. The colour is bluish green and the streak is very pale bluish green. Crystals are transparent with adamantine lustre. The Mohs hardness is estimated at between 2 and 3. Andychristyite is brittle with an irregular fracture and one perfect cleavage on {001}. The calculated density based on the empirical formula is 6.304 g/cm^3. The mineral is optically biaxial, with large 2V, strong dispersion, and moderate very pale blue-green to medium blue-green pleochroism. The electron microprobe analyses (average of five) provided: PbO 43.21, CuO 15.38, TeO_3 35.29, H_2O 3.49 (structure), total 97.37 wt.%. The empirical formula (based on 6 O apfu) is: Pb_(0.98)C u^(2+)_(0.98)Te^(6+)_(1.02)O_6H_(1.96). The Raman spectrum exhibits prominent features consistent with the mineral being a tellurate, as well as an OH stretching feature confirming a hydrous component. The eight strongest powder X-ray diffraction lines are [d_(obs) in Å(I)(hkl)]: 6.71(16)(010), 4.76(17)(110), 3.274(100)(120,102,012), 2.641(27)(102, 211, 112), 2.434(23)(multiple), 1.6736(17)(multiple), 1.5882(21)(multiple) and 1.5133(15)(multiple). The crystal structure of andychristyite (R_1 = 0.0165 for 1511 reflections with Fo > 4σF) consists of stair-step-like hcp polyhedral layers of Te^(6+)O_6 and Cu^(2+)O_6 octahedra parallel to {001}, which are linked in the [001] direction by bonds to interlayer Pb atoms. The structures of eckhardite, bairdite, timroseite and paratimroseite also contain stair-step-like hcp polyhedral layers

Bluebellite and mojaveite, two new minerals from the central Mojave Desert, California, USA

Bluebellite, Cu_6[I^(5+)O_3(OH)_3](OH)_7Cl and mojaveite, Cu_6[Te^(6+)O_4(OH)_2](OH)_7Cl, are new secondary copper minerals from the Mojave Desert. The type locality for bluebellite is the D shaft, Blue Bell claims, near Baker, San Bernardino County, California, while cotype localities for mojaveite are the E pit at Blue Bell claims and also the Bird Nest drift, Otto Mountain, also near Baker. The two minerals are very similar in their properties. Bluebellite is associated particularly with murdochite, but also with calcite, fluorite, hemimorphite and rarely dioptase in a highly siliceous hornfels. It forms bright bluish-green plates or flakes up to ~20 μm ×20 μm ×5 μm in size that are usually curved. The streak is pale bluish green and the lustre is adamantine, but often appears dull because of surface roughness. It is non-fluorescent. Bluebellite is very soft (Mohs hardness ~1), sectile, has perfect cleavage on {001} and an irregular fracture. The calculated density based on the empirical formula is 4.746 g cm^(−3). Bluebellite is uniaxial (–), with mean refractive index estimated as 1.96 from the Gladstone-Dale relationship. It is pleochroic O (bluish green) >> E (nearly colourless). Electron microprobe analyses gave the empirical formula Cu_(5.82)I_(0.99)Al_(0.02)Si_(0.12)O_(3.11)(OH)_(9.80)Cl_(1.09) based on 14 (O+Cl) a.p.f.u. The Raman spectrum shows strong iodate-related bands at 680, 611 and 254 cm^(−1). Bluebellite is trigonal, space group R3, with the unit-cell parameters: a = 8.3017(5), c = 13.259(1) Å, V = 791.4(1) Å^3 and Z = 3. The eight strongest lines in the powder X-ray diffraction (XRD) pattern are [dobs/Å (I) (hkl)]: 4.427(99)(003), 2.664(35)(211), 2.516(100)(212İ), 2.213(9)(006), 2.103(29)(033,214), 1.899(47)(312,215İ), 1.566(48)(140,217) and 1.479(29)(045,143İ,324). Mojaveite occurs at the Blue Bell claims in direct association with cerussite, chlorargyrite, chrysocolla, hemimorphite, kettnerite, perite, quartz and wulfenite, while at the Bird Nest drift, it is associated with andradite, chrysocolla, cerussite, burckhardtite, galena, goethite, khinite, mcalpineite, thorneite, timroseite, paratimroseite, quartz and wulfenite. It has also been found at the Aga mine, Otto Mountain, with cerussite, chrysocolla, khinite, perite and quartz. Mojaveite occurs as irregular aggregates of greenish-blue plates flattened on {001} and often curved, which rarely show a hexagonal outline, and also occurs as compact balls, from sky blue to medium greenish blue in colour. Aggregates and balls are up to 0.5 mm in size. The streak of mojaveite is pale greenish blue, while the lustre may be adamantine, pearly or dull, and it is non-fluorescent. The Mohs hardness is ~1. It is sectile, with perfect cleavage on {001} and an irregular fracture. The calculated density is 4.886 g cm^(−3), based on the empirical formulae and unit-cell dimensions. Mojaveite is uniaxial (–), with mean refractive index estimated as 1.95 from the Gladstone-Dale relationship. It is pleochroic O (greenish blue) >> E (light greenish blue). The empirical formula for mojaveite, based on 14 (O+Cl) a.p.f.u., is Cu_(5.92)Te_(1.00)Pb_(0.08)Bi_(0.01)O_4(OH)_(8.94)Cl_(1.06).The most intense Raman bands occur at 694, 654 (poorly resolved), 624, 611 and 254 cm^(−1). Mojaveite is trigonal, space group R3, with the unit-cell parameters: a = 8.316(2), c = 13.202(6) Å and V = 790.7(1) Å^3. The eight strongest lines in the powder XRD pattern are [d_(obs/) Å (I) (hkl)]: 4.403(91)(003), 2.672(28)(211), 2.512(100)(212İ), 2.110(27)(033,214), 1.889(34)(312,215İ,223İ), 1.570(39)(404,140,217), 1.481(34)(045,143İ,324) and 1.338(14)(422). Diffraction data could not be refined, but stoichiometries and unit-cell parameters imply that bluebellite and mojaveite are very similar in crystal structure. Structure models that satisfy bond-valence requirements are presented that are based on stackings of brucite-like Cu_6MX_(14) layers, where M = (I or Te) and X = (O, OH and Cl). Bluebellite and mojaveite provide a rare instance of isotypy between an iodate containing I^(5+) with a stereoactive lone electron pair and a tellurate containing Te^(6+) with no lone pair

A New Approach to In-situ K-Ar Geochronology

The development of an in-situ geochronology capability for Mars and other planetary surfaces has the potential to fundamentally change our understanding of the evolution of terrestrial bodies in the Solar System. For Mars specifically, many of our most basic scientific questions about the geologic history of the planet require knowledge of the absolute time at which an event or process took place on its surface. For instance, what was the age and rate of early Martian climate change recorded in the mineralogy and morphology of surface lithologies (e.g., [1])? In-situ ages from a few select locations within the globally established stratigraphy of Mars would be transformative, enabling us to place direct chronologic constraints on the timing and rates of impact, volcanic, sedimentary, and aqueous processes on the Martian surface

Camaronesite, [Fe^(3+)(H_2O)_2(PO_3OH)]_2(SO_4)•1-2H_2O, a new phosphate-sulfate from the Camarones Valley, Chile, structurally related to taranakite

Camaronesite (IMA 2012-094), [Fe^(3+)(H_2O)_2(PO_3OH)]_2(SO_4)•1-2H_2O, is a new mineral from near the village of Cuya in the Camarones Valley, Arica Province, Chile. The mineral is a low-temperature, secondary mineral occurring in a sulfate assemblage with anhydrite, botryogen, chalcanthite, copiapite, halotrichite, hexahydrite, hydroniumjarosite, pyrite, römerite, rozenite and szomolnokite. Lavender-coloured crystals up to several mm across form dense intergrowths. More rarely crystals occur as drusy aggregates of tablets up to 0.5 mm in diameter and 0.02 mm thick. Tablets are flattened on {001} and exhibit the forms {001}, {104}, {015} and {018}. The mineral is transparent with white streak and vitreous lustre. The Mohs hardness is 2½, the tenacity is brittle and the fracture is irregular, conchoidal and stepped. Camaronesite has one perfect cleavage on {001}. The measured and calculated densities are 2.43(1) and 2.383 g/cm^3, respectively. The mineral is optically uniaxial (+) with ω = 1.612(1) and ε = 1.621(1) (white light). The pleochroism is O (pale lavender) > E (colourless). Electron-microprobe analyses provided Fe_2O_331.84, P_2O_529.22, SO_315.74, H_2O 23.94 (based on O analyses), total 100.74 wt.%. The empirical formula (based on 2 P a.p.f.u.) is: Fe_(1.94)(PO_3OH)_2(S_(0.96)O_4)(H_2O)_4•1.46H_2O. The mineral is slowly soluble in concentrated HCl and extremely slowly soluble in concentrated H_2SO_4. Camaronesite is trigonal, R32, with cell parameters:a = 9.0833(5), c = 42.944(3) Å, V = 3068.5(3) Å3 and Z = 9. The eight strongest lines in the X-ray powder diffraction pattern are [d_(obs) Å (I)(hkl)]: 7.74(45)(101), 7.415(100)(012), 4.545(72)(110), 4.426(26)(018), 3.862(32)(021,202,116), 3.298(93)(027,119), 3.179(25)(208) and 2.818(25)(1•1•12,125). In the structure of camaronesite (R_1 = 2.28% for 1138 F_o > 4σF), three types of Fe octahedra are linked by corner sharing with (PO_3OH) tetrahedra to form polyhedral layers perpendicular to c with composition [Fe^(3+)(H_2O)_2(PO_3OH)]. Two such layers are joined through SO_4 tetrahedra (in two half-occupied orientations) to form thick slabs of composition [Fe^(3+)(H_2O)_2(PO_3OH)]_2(SO_4). Between the slabs are partially occupied H_2O groups. The only linkages between the slabs are hydrogen bonds. The most distinctive component in the structure consists of two Fe octahedra linked to one another by three PO_4 tetrahedra yielding an [Fe_2(PO_4)_3] unit. This unit is also the key component in the sodium super-ionic conductor (NASICON) structure and has been referred to as the lantern unit. The polyhedral layers in the structure of camaronesite are similar to those in the structure of taranakite. The Raman spectrum exhibits peaks consistent with sulfate, phosphate, water and OH groups

Targeting mitochondrial fitness as a strategy for healthy vascular aging.

Cardiovascular diseases (CVD) are the leading cause of death worldwide and aging is the primary risk factor for CVD. The development of vascular dysfunction, including endothelial dysfunction and stiffening of the large elastic arteries (i.e., the aorta and carotid arteries), contribute importantly to the age-related increase in CVD risk. Vascular aging is driven in large part by oxidative stress, which reduces bioavailability of nitric oxide and promotes alterations in the extracellular matrix. A key upstream driver of vascular oxidative stress is age-associated mitochondrial dysfunction. This review will focus on vascular mitochondria, mitochondrial dysregulation and mitochondrial reactive oxygen species (ROS) production and discuss current evidence for prevention and treatment of vascular aging via lifestyle and pharmacological strategies that improve mitochondrial health. We will also identify promising areas and important considerations ('research gaps') for future investigation.REVIEW ARTICLE| JUNE 25 2020 Targeting mitochondrial fitness as a strategy for healthy vascular aging Matthew J. Rossman ; Rachel A. Gioscia-Ryan ; Zachary S. Clayton ; Michael P. Murphy ; Douglas R. Seals Crossmark: Check for Updates Clin Sci (Lond) (2020) 134 (12): 1491–1519. https://doi.org/10.1042/CS20190559 Article history Split-Screen Views Icon Views PDF Link PDF Share Icon Share Cite Icon Cite Get Permissions Abstract Cardiovascular diseases (CVD) are the leading cause of death worldwide and aging is the primary risk factor for CVD. The development of vascular dysfunction, including endothelial dysfunction and stiffening of the large elastic arteries (i.e., the aorta and carotid arteries), contribute importantly to the age-related increase in CVD risk. Vascular aging is driven in large part by oxidative stress, which reduces bioavailability of nitric oxide and promotes alterations in the extracellular matrix. A key upstream driver of vascular oxidative stress is age-associated mitochondrial dysfunction. This review will focus on vascular mitochondria, mitochondrial dysregulation and mitochondrial reactive oxygen species (ROS) production and discuss current evidence for prevention and treatment of vascular aging via lifestyle and pharmacological strategies that improve mitochondrial health. We will also identify promising areas and important considerations (‘research gaps’) for future investigation. Keywords:arterial stiffness, endothelial function, mitophagy, oxidative stress, reactive oxygen species Subjects:Aging, Cardiovascular System & Vascular Biology, Translational Science Cardiovascular diseases (CVD) remain the largest contributor to morbidity and mortality in both developed and many developing nations [1,2]. Aging is by far the strongest risk factor for CVD, with >90% of all deaths occurring in adults 50 years of age and older [1,2]. Importantly, the changing demographics of aging characterized by a shift toward older populations [3] predicts a progressive, marked increase in prevalence of CVD in the absence of effective intervention [4]. A key mechanism by which aging increases CVD risk is the development of vascular dysfunction [5,6]. A number of adverse changes to the vasculature occur with aging, but two major clinically relevant expressions are endothelial dysfunction, as assessed by reduced arterial dilation in response to endothelium-derived nitric oxide (NO), and stiffening of the large elastic arteries (i.e., the aorta and carotid arteries) [5,6]. In combination, endothelial dysfunction and arterial stiffening contribute to a ‘vascular aging’ phenotype that drives much of the adverse effects of age on CVD. Vascular endothelial dysfunction The vascular endothelium is a single-cell layer lining the lumen of blood vessels. Endothelial cells play a critical role regulating vasomotor tone, metabolism, immune function, thrombosis and many other processes via synthesis and release of a variety of vasoactive molecules [7]. A major vasodilatory and largely vasoprotective molecule released by endothelial cells is NO, which is produced in response to mechanical (i.e., blood flow) and chemical (e.g., acetylcholine [ACh]) stimuli by the enzyme nitric oxide synthase (eNOS); eNOS catalyzes the generation of NO from L-arginine and oxygen, with NO subsequently diffusing to vascular smooth muscle cells where it induces vascular smooth muscle relaxation and vasodilation [7]. Endothelial dysfunction occurs with aging and is characterized by a decline in endothelium-dependent dilation (EDD), largely as a consequence of reductions in NO, although changes in concentrations of vasoactive factors such as prostaglandins, endothelin-1, norepinephrine and angiotensin II also contribute [7]. NO-mediated EDD can be determined in pre-clinical models by assessing changes in artery diameter in response to flow in vivo [8,9] or changes in diameter of isolated artery segments ex vivo in response to mechanical or pharmacological stimuli, such as ACh [10]. In humans, the gold-standard non-invasive assessment of NO-mediated EDD is brachial artery flow-mediated dilation (FMD), in which the change in brachial artery diameter in response to increases in blood flow is determined [10,11]. Brachial artery FMD primarily assesses macrovascular (conduit artery) function. Microvascular (resistance vessel) function can be determined by measuring changes in blood flow in response to intra-arterial infusions of ACh and is primarily assessed in the forearm [10,11]. These experimental approaches all demonstrate reduced endothelial function with aging in pre-clinical models and humans [12–17]. Endothelial dysfunction is the major antecedent of atherosclerosis [5,18] and both reduced brachial artery FMD and lower forearm blood flow responses to ACh are independent predictors of CV events and CVD in middle-aged and older adults free from clinical disease in large, community-based cohort studies [19–21]. Large elastic artery stiffening The aorta and carotid arteries expand and recoil as blood is ejected into the arterial system by the left ventricle during systole [22]. This action limits arterial pulsatile pressures by providing a dampening function and protects the downstream microvasculature from potentially damaging fluctuations in blood pressure and flow [23]. Moreover, the elastic recoil of the aorta aids in the propulsion of blood to the periphery and maintains perfusion of the heart during diastole [22]. With aging, aortic stiffening results in blood being ejected into a stiffer aorta, which augments central systolic blood pressure because the ejected pressure wave travels at a higher velocity in stiffer arteries and is reflected by points of impedance such that the returning pressure wave reaches the heart at mid-to-late systole [22,24]. In addition, the greater forward moving pressure wave amplitude (from systolic ejection, prior to the return of wave reflections) is a major contributor to the age-related increase in central systolic blood pressure after age 60, particularly in women, as a consequence of a plateau or decrease in reflected wave amplitude [25,26]. The augmented systolic blood pressure, in turn, contributes to isolated systolic hypertension and results in a loss of diastolic pressure augmentation, such that aortic pulse pressure is widened [22,24]. Aortic stiffening therefore increases left ventricular afterload during systole, promoting left ventricular hypertrophy and dysfunction, and compromises coronary perfusion during diastole because of the reduced augmentation of diastolic pressure [24,27]. The loss of pulsatility-dampening effects of the aorta and the carotid artery also allows for transmission of high pulsatile pressures to the delicate small vessels in the microcirculation, which is particularly harmful for high-flow, low-resistance organs such as the brain and kidney, and a potential causative factor in target organ damage [23]. Structural changes to arteries, functional influences (i.e., factors influencing vascular smooth muscle tone) and the stiffness of vascular smooth muscle cells contribute to large elastic artery stiffening with aging [28,29]. The primary structural changes mediating arterial stiffening occur in the extracellular matrix and include degradation/fragmentation of elastin (e.g., by matrix metalloproteinases), an increase in the deposition of collagen and formation of advanced glycation end products (AGEs), which cross-link collagen fibers, increasing their stiffness [5,30,31]. Increased vascular smooth muscle tone is a consequence of changes such as reductions in NO and increased sympathetic nervous system, endothelin-1 and renin–angiotensin aldosterone system activity [32–34]. These factors also influence the intrinsic stiffness of the vascular smooth muscle cells, which adds to the stiffness of the arterial wall [29]. The mechanical stiffness of the large elastic arteries can be determined ex vivo in pre-clinical models by directly measuring properties such as compliance by creating stress-strain curves [35,36]. In vivo, arterial stiffness can be assessed in pre-clinical settings and humans with pulse wave velocity (PWV), which is a measure of the (regional) speed of the pulse wave generated by the heart when blood is ejected into the arterial system [22]. Aortic PWV is the predominant measure in rodents and carotid-femoral PWV is the reference standard measure of aortic stiffness in humans [10,22]. Carotid-femoral PWV increases with aging and is a strong, independent predictor of CVD risk in older adults [37,38]. Moreover, consistent with aortic stiffness-associated end organ damage, growing evidence supports an association between elevated carotid-femoral PWV and other age-related clinical disorders such as cognitive decline, dementia, including Alzheimer’s disease, and decreases in renal function/chronic kidney disease [39–43]. The local distensibility of the carotid artery can also be determined in humans by measuring carotid artery compliance (the change in artery diameter for a given change in arterial pressure) and determining the carotid distensibility coefficient (i.e., changes in artery diameter normalized to diastolic lumen diameter) and/or carotid beta-stiffness index, which is largely independent of blood pressure [10,22]. Carotid artery compliance is associated with incident stroke, independent of aortic stiffness [44]. Mechanisms of vascular dysfunction with aging The primary molecular mechanisms of vascular aging are oxidative stress and chronic, low grade inflammation [45,46] (Figure 1). Excessive production of reactive oxygen species (ROS) in combination with unchanged or decreased abundance/activity of antioxidant enzymes (e.g., superoxide dismutase, SOD) results in the development of oxidative stress in arteries with aging [24,45]. Excess superoxide rapidly reacts with NO to form the secondary reactive species peroxynitrite (ONOO−), decreasing the bioavailability of NO [24,45], causing endothelial dysfunction. Peroxynitrite is also the primary molecule that reacts with and oxidizes tetrahydrobiopterin (BH4), an essential co-factor for NO production by eNOS [47]. Loss of BH4 leads to eNOS uncoupling, whereby eNOS produces more superoxide and less NO, exacerbating oxidative stress and decreasing bioavailable NO and endothelial cell function [47]. Excess ROS also can activate pro-inflammatory networks such as those regulated by the transcription factor nuclear factor kappa B (NF-kB), which up-regulates the production of pro-inflammatory cytokines that can impair vascular function and activate other ROS producing systems and enzymes, creating an adverse feed-forward (vicious) cycle of inflammation and oxidative stress [24,45]. Figure 1 Aging is associated with mitochondrial dysfunction-induced increases in reactive oxygen species (ROS) and oxidative stress and increases in pro-inflammatory cytokine signaling and chronic low-grade inflammation. Together, these processes induce vascular dysfunction, featuring: (lower left) large elastic artery stiffening mediated by degradation of elastin fibers (blue), increased deposition of collagen (brown), and greater cross-linking of structural proteins by advanced glycation end-products (dashed connecting lines); and (right) vascular endothelial dysfunction characterized by reduced nitric oxide (NO) bioavailability and endothelium-dependent dilation. These and other changes to arteries, in turn, increase the risk of developing cardiovascular diseases, chronic kidney disease, and Alzheimer’s disease and related dementias. VIEW LARGEDOWNLOAD SLIDE Mechanisms of age-associated vascular dysfunction and related clinical disorders Aging is associated with mitochondrial dysfunction-induced increases in reactive oxygen species (ROS) and oxidative stress and increases in pro-inflammatory cytokine signaling and chronic low-grade inflammation. Together, these processes induce vascular dysfunction, featuring: (lower left) large elastic artery stiffening mediated by degradation of elastin fibers (blue), increased deposition of collagen (brown), and greater cross-linking of structural proteins by advanced glycation end-products (dashed connecting lines); and (right) vascular endothelial dysfunction characterized by reduced nitric oxide (NO) bioavailability and endothelium-dependent dilation. These and other changes to arteries, in turn, increase the risk of developing cardiovascular diseases, chronic kidney disease, and Alzheimer’s disease and related dementias. This overall state of oxidative stress and inflammation also contributes to arterial stiffening with aging by altering the structural properties of the arterial wall. Production of collagen by fibroblasts is stimulated by superoxide-related oxidative stress [30,48,49]. Matrix metalloproteinases are up-regulated and elastin content is lower in aorta of SOD-deficient mice, consistent with the concept that elastin degradation is induced by oxidative stress [50]. Vascular oxidative stress also promotes transforming growth factor β signaling and this, in turn, stimulates inflammation, which further reinforces arterial stiffness via activation of the pro-oxidant enzyme, NADPH oxidase [48]. AGEs interact with the receptor for AGEs to activate NFkB-regulated pro-inflammatory pathways and oxidative stress, which ultimately perpetuates arterial stiffening and further increases production of AGEs [51]. Mitochondrial dysfunction is emerging as a key source of vascular oxidative stress and contributor to age-related vascular dysfunction. The remaining sections of this article will focus on mitochondrial dysfunction as a driver of vascular aging and review current evidence for prevention/treatment of age-associated vascular dysfunction via lifestyle and pharmacological strategies that improve mitochondrial health. We will also discuss current ‘research gaps’ and future directions for the field. Vascular mitochondria, mitochondrial dysregulation and ROS Mitochondria are cytoplasmic organelles that are present in the majority of cell types in the human body, including vascular endothelial and smooth muscle cells. Mitochondria are often referred to as the ‘powerhouse’ of the cell for their role in ATP production by oxidative phosphorylation, which occurs via a series of electron transfers through the respiratory chain in the mitochondrial inner membrane that is coupled to ATP synthesis by the FoF1-ATP synthase by the protonmotive force across the inner membrane. However, mitochondria are also vital for a number of additional cellular processes, including regulation of metabolism, calcium homeostasis, immune function, cell growth and stem cell function, and cell death pathways. Although mitochondrial density in vascular tissues is considerably lower than other tissues such as skeletal muscle, liver and heart [52,53], increasing evidence indicates that these organelles are critical for maintenance of cellular and tissue homeostasis in the vasculature. This topic has been reviewed in detail elsewhere [54–61], but below we briefly summarize some of the key roles of mitochondria in the vasculature. A first important distinction is to consider the vascular cell type in question, as the density and subcellular distribution of mitochondria vary between endothelial and vascular smooth muscle cells, and indeed even among the same cell types in different vascular beds [54,60]. In general, unlike in highly metabolically active tissues with greater ATP demand, the principal role of mitochondria in the vasculature appears to be cellular signaling rather than energy provision [54]. Cellular energy demand is quite low in endothelial cells, and ATP demand is met primarily via glycolysis. However, endothelial mitochondria are critical in the regulation of calcium homeostasis, apoptosis/necrosis, cellular response to stress, and immune and inflammatory pathways. An essential feature of these roles is the regulated production of signaling molecules including redox-active molecules (reactive oxygen, nitrogen and other species; mtROS), mitochondrial DNA, mitochondria-derived peptides and damage-associated molecular pattern molecules (DAMPs), which exert effects intra- and extra-cellularly [62]. Importantly, there is cross-talk between mitochondrial and nuclear signaling pathways, whereby mitochondria-derived signaling is both influenced by and can influence nuclear events including gene expression [63]. Similarly, in vascular smooth muscle cells, mitochondria have an important role in cellular signaling. Mitochondria are involved in signaling pathways for regulation of vascular smooth muscle cell growth and proliferation (e.g., TGF-β activity) [64], as well as maintenance of the dynamic balance among synthesis and breakdown of extracellular structural proteins, including collagen and elastin (e.g., matrix metalloproteinase enzyme activities) [65]. There is also emerging evidence demonstrating interplay between mtROS signaling and inflammatory pathways known to be important for regulating vascular smooth muscle cell function, including those involving NFkB and the NLRP3-inflammasome [66–69], further highlighting the crucial role of mtROS in vascular homeostasis. Mitochondrial ROS The signaling functions of vascular mitochondria are thought to be mediated in large part by the production of ROS at low, physiological levels. However, the dysregulation of this mtROS production also has the potential to lead to pathophysiological sequelae that disrupt other mitochondrial functions, cellular homeostasis, and ultimately vascular function. The production of ROS by mitochondria can occur at several sites (Figure 2), including but not limited to the electron transport proteins, and this topic has been reviewed in detail elsewhere [54,60,70]. The most important sites for ROS production within mitochondria appear to be complexes I and III. These ROS are thought to be critical transducers of signaling mediated by mitochondria, leading to post-transcriptional modification of proteins and interactions with immune and inflammatory cellular pathways, although the mechanistic details are still uncertain. In the vasculature, the proximal mtROS species is superoxide, which is generated primarily at the electron transport chain in the mitochondrial inner membrane via interaction between oxygen and unpaired electrons, influenced by the proton motive force and the redox state of the coenzyme Q pool and integrity of intrinsic electron transport chain proteins [54,58,60,70]. Superoxide is released into the matrix (complex I) or into both the matrix and intermembrane space (complex III); it can also undergo dismutation to hydrogen peroxide by the antioxidant enzyme manganese superoxide dismutase (MnSOD) [59,60,62,70]. Hydrogen peroxide is also generated de novo on the surface of the mitochondrial outer membrane or in the intermembrane space mitochondria by p66SHC, a growth factor adapter protein referred to as a sensor/marker and ‘master regulator’ of mitochondrial redox signaling whose activity is indicative of the rate of mtROS production [71]. In addition, NADPH oxidase 4 (NOX4) is viewed as a primarily mitochondrial isoform of the NOX monoamine oxidase family of enzymes that contributes to mitochondrial hydrogen peroxide generation [72], although more research is needed to confirm the mitochondrial specificity of NOX4. Figure 2 Aging is associated with dysregulated mitochondrial quality control featuring reduced mitochondrial biogenesis (upper left) and reduced mitophagy (upper right), increased mitochondrial fission (upper middle right), reduced mitochondrial fusion (lower middle right), reduced mitochondrial stress resistance (lower right), increased mitochondrial DNA damage (middle left of mitochondria image) and increased bioactivity of mitochondrial reactive oxygen species (e.g., superoxide and other reactive oxygen species [ROS], middle of mitochondria image) relative to antioxidant defenses (e.g., manganese superoxide dismutase [SOD], lower right of mitochondria). VIEW LARGEDOWNLOAD SLIDE Mechanisms of age-associated mitochondrial dysfunction Aging is associated with dysregulated mitochondrial quality control featuring reduced mitochondrial biogenesis (upper left) and reduced mitophagy (upper right), increased mitochondrial fission (upper middle right), reduced mitochondrial fusion (lower middle right), reduced mitochondrial stress resistance (lower right), increased mitochondrial DNA damage (middle left of mitochondria image) and increased bioactivity of mitochondrial reactive oxygen species (e.g., superoxide and other reactive oxygen species [ROS], middle of mitochondria image) relative to antioxidant defenses (e.g., manganese superoxide dismuta

Joteite, Ca_2CuAl[AsO_4][AsO_3(OH)]_2(OH)_2•5H_2O, a new arsenate with a sheet structure and unconnected acid arsenate groups

Joteite (IMA2012-091), Ca_2CuAl[AsO_4][AsO_3(OH)]_2(OH)_2•5H_2O, is a new mineral from the Jote mine, Tierra Amarilla, Copiapó Province, Atacama, Chile. The mineral is a late-stage, lowtemperature, secondary mineral occurring with conichalcite, mansfieldite, pharmacoalumite, pharmacosiderite and scorodite in narrow seams and vughs in the oxidized upper portion of a hydrothermal sulfide vein hosted by volcanoclastic rocks. Crystals occur as sky-blue to greenish-blue thin blades, flattened and twinned on {001}, up to ~300 µm in length, and exhibiting the forms {001}, {010}, {110}, {210} and {111}. The blades are commonly intergrown in wheat-sheaf-like bundles, less commonly in sprays, and sometimes aggregated as dense crusts and cavity linings. The mineral is transparent and has a very pale blue streak and vitreous lustre. The Mohs hardness is estimated at 2 to 3, the tenacity is brittle, and the fracture is curved. It has one perfect cleavage on {001}. The calculated density based on the empirical formula is 3.056 g/cm^3. It is optically biaxial (–) with α = 1.634(1), β = 1.644(1), γ = 1.651(1) (white light), 2V_(meas) = 78(2)° and 2V_(calc) = 79.4°. The mineral exhibits weak dispersion, r Y (pale greenish blue) > X (colourless). The normalized electron-microprobe analyses (average of 5) provided: CaO 15.70, CuO 11.22, Al_2O_38.32, As_2O_546.62, H_2O 18.14 (structure), total 100 wt.%. The empirical formula (based on 19 O a.p.f.u.) is: Ca_(1.98)Cu_(1.00)Al_(1.15)As_(2.87)H_(14.24)O_(19). The mineral is slowly soluble in cold, concentrated HCl. Joteite is triclinic, P1, with the cell parameters: a = 6.0530(2), b = 10.2329(3), c = 12.9112(4) Å, a = 87.572(2), b = 78.480(2), g = 78.697(2)°, V = 768.40(4) Å^3 and Z = 2. The eight strongest lines in the X-ray powder diffraction pattern are [d_(obs) Å (I)(hkl)]: 12.76(100)(001), 5.009(23)(020), 4.206(26)(120,003,121), 3.92(24)(022,022,102), 3.40(25)(113), 3.233(19)(031,023,123,023), 2.97(132,201) and 2.91(15)(122,113). In the structure of joteite (R_1 = 7.72% for 6003 F_o > 4σF), AsO_4 and AsO_3 (OH) tetrahedra, AlO_6 octahedra and Cu^(2+)O_5 square pyramids share corners to form sheets parallel to {001}. In addition, 7- and 8-coordinate Ca polyhedra link to the periphery of the sheets yielding thick slabs. Between the slabs are unconnected AsO_3(OH) tetrahedra, which link the slabs only via hydrogen bonding. The Raman spectrum shows features consistent with OH and/or H_2O in multiple structural environments. The region between the slabs may host excess Al in place of some As